Blood Pressure and Functional Recovery in Acute Ischemic Stroke

Neurology Service/IDIBAPS, Hospital Clínic, Barcelona, Spain.
Stroke (Impact Factor: 5.72). 09/1998; 29(9):1850-3. DOI: 10.1016/S0895-7061(01)01591-6
Source: PubMed


The relevance of elevated blood pressure in acute ischemic stroke and its most appropriate management are unresolved. We aimed to evaluate the rate of functional recovery with relation to early blood pressure management in patients with ischemic stroke.
Four hundred eighty-one consecutive ischemic stroke patients were admitted to the Neurology Service within 20.9+/-10.5 hours of symptoms onset as part of the Barcelona Downtown Stroke Registry, including 235 patients who received oral antihypertensive agents within <24 hours after stroke onset. Demographic, clinical (Mathew scale), and CT scan findings were collected prospectively. Mean arterial pressure (MAP) was recorded before hospital arrival and at 7 AM on days 1, 2, and 7 of hospitalization. The primary end point was complete functional recovery at day 7 defined as a score of 0 to 1 on the modified Rankin scale.
Two hundred fifty-two patients achieved complete recovery on day 7. Using logistic regression, independent predictors of complete recovery included mild impairment at stroke presentation, lack of history of hypertension, and absence of brain edema on CT scan. Also, a 20% to 30% drop in MAP on day 2 after stroke onset almost tripled the odds of full recovery (odds ratio, 2.9; 95% CI, 1.3 to 6.3). MAP tended to normalize after stroke in all subjects, more rapidly if hypotensive agents were administered. Brain edema was also less frequent in patients with a greater drop in blood pressure. Despite the fact that a drop in MAP >30% from baseline was observed in 49 patients, this preceded worsening stroke in only 4 patients. Conversely, worsening stroke occurred in 51 patients despite stable blood pressure.
These results suggest that complete recovery in ischemic stroke is facilitated by a moderate blood pressure reduction when brain edema develops, most likely as the result of a more adequate cerebral perfusion pressure. Conversely, stroke worsening due to pharmacological hypoperfusion is exceptional.

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Available from: Angel Chamorro, Oct 07, 2015
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    • "The Barcelona Downtown stroke registry found that early decrease of systolic blood pressure by 20–30% was associated with full recovery (OR 2.9, 95% CI 1.3–6.3) [16]. A decrease in systolic blood pressure within 12 hours was associated with recanalization of the vessel [18]. "
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    ABSTRACT: High blood pressure is common in acute stroke patients. Very high as well as very low blood pressure is associated with poor outcome. Spontaneous fall of blood pressure within the first few days after stroke was associated both with neurological improvement and impairment. Several randomized trials investigated the pharmacological reduction of blood pressure versus control. Most trials showed no significant difference in their primary outcome apart from the INWEST trial which found an increase of poor outcome when giving intravenous nimodipine. Nevertheless, useful information can be extracted from the published data to help guide the clinician's decision. Blood pressure should only be lowered when it is clearly elevated, and early after onset, reduction should be moderate but may be achieved rapidly. No clear recommendations can be given on the substances to use; however, care should be taken with intravenous calcium channel blockers and angiotensin receptor antagonists. Two ongoing randomized trials will help to solve the questions on blood pressure management in acute stroke.
    International Journal of Hypertension 04/2013; 2013:349782. DOI:10.1155/2013/349782
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    • "13, 14, 15, 16 This increased blood pressure (BP) falls spontaneously within the first week, without specific antihypertensive therapy.17 Severe hypertension in the early phase of acute ischemic stroke is another sign associated with poor functional outcome and higher mortality.18, 19, 20 As yet, however, there are only limited data on the association of SAP with severe arterial hypertension in patients with acute stroke. "
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    ABSTRACT: Pneumonia is one of the most frequent complications in elderly patients with acute ischemic stroke. Although severe hypertension is often observed in the early phase of acute stroke, there are few studies of acute hypertension as a factor influencing the incidence of stroke-associated pneumonia (SAP) in elderly subjects with acute ischemic stroke. To assess the association of acute phase blood-pressure elevation with the incidence of SAP, we compared 10 elderly patients with acute ischemic stroke complicated with severe hypertension (≥ 200/120 mm Hg) with 43 patients with moderate hypertension (160-199/100-119 mm Hg), as well as with 65 control normotensive or mildly hypertensive (<160/100 mm Hg) controls on admission. Data were collected on known risk factors, type of ischemic stroke and underlying chronic conditions. The significance of differences in risk factors was analyzed using univariate and multivariate comparisons of 38 SAP cases and others, 8 SAP death cases and others, and 28 patients with poor outcome associated with in-hospital death or artificial feeding at discharge and others. After adjustment for potential confounding factors, the relative risk estimates for SAP, SAP death and poor outcome were 2.83 (95% confidence interval 1.14-7.05), 5.20 (1.01-26.8) and 6.84 (1.32-35.4), respectively, for severe hypertension relative to normotensive or mildly hypertensive controls. We conclude that severe hypertension on admission is an independent predictive factor for SAP in elderly patients with acute ischemic stroke.
    Hypertension Research 02/2012; 35(6):648-53. DOI:10.1038/hr.2012.7 · 2.66 Impact Factor
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    • "As a consequence, AS is a specific state of risk (Parmeggiani, 1991). Moreover, between 10 and 40% of strokes occur during the night (Marshall, 1977; van der Windt & van Gijn, 1988; Chamorro et al. 1998; Basetti & Aldrich, 1999), and a low blood pressure may contribute to night-time stroke (Basetti & Aldrich, 1999). This study was designed to assess the cerebral circulation's ability to respond to hypotension during sleep. "
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    ABSTRACT: Autoregulation is a vital protective mechanism that maintains stable cerebral blood flow as cerebral perfusion pressure changes. We contrasted cerebral autoregulation across sleep-wake states, as little is known about its effectiveness during sleep. Newborn lambs (n= 9) were instrumented to measure cerebral blood flow (flow probe on the superior sagittal sinus) and cerebral perfusion pressure, then studied during active sleep (AS), quiet sleep (QS) and quiet wakefulness (QW). We generated cerebral autoregulation curves by inflating an occluder cuff around the brachiocephalic artery thereby lowering cerebral perfusion pressure. Baseline cerebral blood flow was higher (P < 0.05) and cerebral vascular resistance lower (P < 0.05) in AS than in QW (76 +/- 8% and 133 +/- 15%, respectively, of the AS value, mean +/-s.d.) and in QS (66 +/- 11% and 158 +/- 30%). The autoregulation curve in AS differed from that in QS and QW in three key respects: firstly, the plateau was elevated relative to QS and QW (P < 0.05); secondly, the lower limit of the curve (breakpoint) was higher (P < 0.05) in AS (50 mmHg) than QS (45 mmHg); and thirdly, the slope of the descending limb below the breakpoint was greater (P < 0.05) in AS than QS (56% of AS) or QW (56% of AS). Although autoregulation functions in AS, the higher breakpoint and greater slope of the descending limb may place the brain at risk for vascular compromise should hypotension occur.
    The Journal of Physiology 05/2005; 564(Pt 3):923-30. DOI:10.1113/jphysiol.2005.083352 · 5.04 Impact Factor
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